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Article ; Online: The effect of GLP-1 receptor agonist lixisenatide on experimental diabetic retinopathy.

Oezer, Kuebra / Kolibabka, Matthias / Gassenhuber, Johann / Dietrich, Nadine / Fleming, Thomas / Schlotterer, Andrea / Morcos, Michael / Wohlfart, Paulus / Hammes, Hans-Peter

Acta diabetologica

2023 Volume 60, Issue 11, Page(s) 1551–1565

Abstract: Aims: Glucagon-like peptide-1 receptor agonists are effective treatments for type 2 diabetes, effectively lowering glucose without weight gain and with low risk for hypoglycemia. However, their influence on the retinal neurovascular unit remains unclear. ...

Abstract	Aims: Glucagon-like peptide-1 receptor agonists are effective treatments for type 2 diabetes, effectively lowering glucose without weight gain and with low risk for hypoglycemia. However, their influence on the retinal neurovascular unit remains unclear. In this study, we analyzed the effects of the GLP-1 RA lixisenatide on diabetic retinopathy. Methods: Vasculo- and neuroprotective effects were assessed in experimental diabetic retinopathy and high glucose-cultivated C. elegans, respectively. In STZ-diabetic Wistar rats, acellular capillaries and pericytes (quantitative retinal morphometry), neuroretinal function (mfERG), macroglia (GFAP western blot) and microglia (immunohistochemistry) quantification, methylglyoxal (LC-MS/MS) and retinal gene expressions (RNA-sequencing) were determined. The antioxidant properties of lixisenatide were tested in C. elegans. Results: Lixisenatide had no effect on glucose metabolism. Lixisenatide preserved the retinal vasculature and neuroretinal function. The macro- and microglial activation was mitigated. Lixisenatide normalized some gene expression changes in diabetic animals to control levels. Ets2 was identified as a regulator of inflammatory genes. In C. elegans, lixisenatide showed the antioxidative property. Conclusions: Our data suggest that lixisenatide has a protective effect on the diabetic retina, most likely due to a combination of neuroprotective, anti-inflammatory and antioxidative effects of lixisenatide on the neurovascular unit.
MeSH term(s)	Rats ; Animals ; Diabetic Retinopathy/drug therapy ; Diabetic Retinopathy/etiology ; Diabetic Retinopathy/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Hypoglycemic Agents/pharmacology ; Hypoglycemic Agents/therapeutic use ; Glucagon-Like Peptide-1 Receptor/agonists ; Caenorhabditis elegans ; Chromatography, Liquid ; Rats, Wistar ; Diabetes Mellitus, Experimental/drug therapy ; Diabetes Mellitus, Experimental/metabolism ; Tandem Mass Spectrometry ; Antioxidants/pharmacology ; Glucose
Chemical Substances	lixisenatide (74O62BB01U) ; Hypoglycemic Agents ; Glucagon-Like Peptide-1 Receptor ; Antioxidants ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2023-07-09
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1097676-0
ISSN	1432-5233 ; 0940-5429
ISSN (online)	1432-5233
ISSN	0940-5429
DOI	10.1007/s00592-023-02135-7
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Article: Nearly a Century of Insulin at Sanofi: Looking Back Over the Decades of Production and Development.

Bosnyak, Zsolt / Korn, Marcus / Bielohuby, Maximilian / Wohlfart, Paulus / Tennagels, Norbert

Pediatric endocrinology reviews : PER

2020 Volume 17, Issue Suppl 1, Page(s) 161–169

Abstract: Almost a century ago, the first insulin was produced by Banting, Best, MacLeod and Collip in Toronto, thereby enabling life-saving treatment for people with diabetes. Since then, there have been many advancements in insulin production and development of ... ...

Abstract	Almost a century ago, the first insulin was produced by Banting, Best, MacLeod and Collip in Toronto, thereby enabling life-saving treatment for people with diabetes. Since then, there have been many advancements in insulin production and development of new insulin analogues. In this article, we reflect on the rich heritage of Sanofi and its predecessor, Hoechst, in insulin production and development, from being one of the first companies to produce insulin in Europe in 1923, to modern-day insulin analogues and integrated care solutions at present-day Sanofi.
MeSH term(s)	Diabetes Mellitus/drug therapy ; Humans ; Hypoglycemic Agents ; Insulin/supply & distribution
Chemical Substances	Hypoglycemic Agents ; Insulin
Language	English
Publishing date	2020-03-21
Publishing country	Israel
Document type	Journal Article
ZDB-ID	2434390-0
ISSN	1565-4753
ISSN	1565-4753
DOI	10.17458/per.vol17.2020.bkb.sanoficenturyinsulin
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Article: ET-CORM Mediated Vasorelaxation of Small Mesenteric Arteries: Involvement of Kv7 Potassium Channels.

Zhang, Danfeng / Krause, Bernhard M / Schmalz, Hans-Günther / Wohlfart, Paulus / Yard, Benito A / Schubert, Rudolf

Frontiers in pharmacology

2021 Volume 12, Page(s) 702392

Abstract: Although the vasoactive properties of carbon monoxide (CO) have been extensively studied, the mechanism by which CO mediates vasodilation is not completely understood. Through-out published studies on CO mediated vasodilation there is inconsistency on ... ...

Abstract	Although the vasoactive properties of carbon monoxide (CO) have been extensively studied, the mechanism by which CO mediates vasodilation is not completely understood. Through-out published studies on CO mediated vasodilation there is inconsistency on the type of K
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2021.702392
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Article ; Online: Activation of thyroid hormone receptor-β improved disease activity and metabolism independent of body weight in a mouse model of non-alcoholic steatohepatitis and fibrosis.

Kannt, Aimo / Wohlfart, Paulus / Madsen, Andreas Nygaard / Veidal, Sanne Skovgård / Feigh, Michael / Schmoll, Dieter

British journal of pharmacology

2021 Volume 178, Issue 12, Page(s) 2412–2423

Abstract: Background and purpose: Activation of hepatic thyroid hormone receptor β (THR-β) is associated with systemic lipid lowering, increased bile acid synthesis, and fat oxidation. In patients with non-alcoholic steatohepatitis (NASH), treatment with THR-β ... ...

Abstract	Background and purpose: Activation of hepatic thyroid hormone receptor β (THR-β) is associated with systemic lipid lowering, increased bile acid synthesis, and fat oxidation. In patients with non-alcoholic steatohepatitis (NASH), treatment with THR-β agonists decreased hepatic steatosis and circulating lipids, and induced resolution of NASH. We chose resmetirom (MGL-3196), a liver-directed, selective THR-β agonist, as a prototype to investigate the effects of THR-β activation in mice with diet-induced obesity (DIO) and biopsy-confirmed advanced NASH with fibrosis. Experimental approach: C57Bl/6J mice were fed a diet high in fat, fructose, and cholesterol for 34 weeks, and only biopsy-confirmed DIO-NASH mice with fibrosis were included. Resmetirom was administered at a daily dose of 3 mg·kg Key results: Treatment with resmetirom did not influence body weight but led to significant reduction in liver weight, hepatic steatosis, plasma alanine aminotransferase activity, liver and plasma cholesterol, and blood glucose. These metabolic effects translated into significant improvement in NAFLD activity score. Moreover, a lower content of α-smooth muscle actin and down-regulation of genes involved in fibrogenesis indicated a decrease in hepatic fibrosis. Conclusion and implications: Our model robustly reflected clinical observations of body weight-independent improvements in systemic and hepatic metabolism including anti-steatotic activity.
MeSH term(s)	Animals ; Diet, High-Fat ; Disease Models, Animal ; Humans ; Liver/pathology ; Liver Cirrhosis/drug therapy ; Liver Cirrhosis/pathology ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease/drug therapy ; Non-alcoholic Fatty Liver Disease/pathology ; Obesity/pathology ; Thyroid Hormone Receptors beta/genetics
Chemical Substances	Thyroid Hormone Receptors beta
Language	English
Publishing date	2021-04-06
Publishing country	England
Document type	Journal Article
ZDB-ID	80081-8
ISSN	1476-5381 ; 0007-1188
ISSN (online)	1476-5381
ISSN	0007-1188
DOI	10.1111/bph.15427
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Article ; Online: Concentration-dependent effects of dichloroacetate in type 2 diabetic hearts assessed by hyperpolarized [1-

Hansen, Esben Søvsø Szocska / Bertelsen, Lotte Bonde / Bøgh, Nikolaj / Miller, Jack / Wohlfart, Paulus / Ringgaard, Steffen / Laustsen, Christoffer

NMR in biomedicine

2022 Volume 35, Issue 6, Page(s) e4678

Abstract: Personalized medicine or individualized therapy promises a paradigm shift in healthcare. This is particularly true in complex and multifactorial diseases such as diabetes and the multitude of related pathophysiological complications. Diabetic ... ...

Abstract	Personalized medicine or individualized therapy promises a paradigm shift in healthcare. This is particularly true in complex and multifactorial diseases such as diabetes and the multitude of related pathophysiological complications. Diabetic cardiomyopathy represents an emerging condition that could be effectively treated if better diagnostic and, in particular, better therapeutic monitoring tools were available. In this study, we investigate the ability to differentiate low and high doses of metabolically targeted therapy in an obese type 2 diabetic rat model. Low-dose dichloroacetate (DCA) treatment was associated with increased lactate production, while no or little change was seen in bicarbonate production. High-dose DCA treatment was associated with a significant metabolic switch towards increased bicarbonate production. These findings support further studies using hyperpolarized [1-
MeSH term(s)	Acetates ; Animals ; Bicarbonates ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/diagnostic imaging ; Dichloroacetic Acid/pharmacology ; Dichloroacetic Acid/therapeutic use ; Heart/diagnostic imaging ; Heart/physiology ; Magnetic Resonance Imaging/methods ; Pyruvic Acid/metabolism ; Rats
Chemical Substances	Acetates ; Bicarbonates ; Pyruvic Acid (8558G7RUTR) ; Dichloroacetic Acid (9LSH52S3LQ)
Language	English
Publishing date	2022-01-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1000976-0
ISSN	1099-1492 ; 0952-3480
ISSN (online)	1099-1492
ISSN	0952-3480
DOI	10.1002/nbm.4678
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Zs.A 2869: Show issues

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Article ; Conference proceedings: GPR146 acts as modulator in adipocyte differentiation and homeostasis influencing lipid metabolism in vitro and in vivo

Brachs, Sebastian / Harutyunyan, Aida / Sbierski-Kind, Julia / Kunz, Séverine. / Brachs, Maria / Ehrlich, Lauren / Bielohuby, Maximilian / He, Kaihui Hu / Wohlfart, Paulus / Spranger, Joachim / Mai, Knut

Diabetologie und Stoffwechsel

(Diabetes Kongress 2024 – 58. Jahrestagung der DDG)

2024 Volume 19, Issue S 01

Event/congress	Diabetes. Umwelt. Leben. Perspektiven aus allen Blickwinkeln, CityCube Berlin, 2024-05-08
Series title	Diabetes Kongress 2024 – 58. Jahrestagung der DDG
Language	German
Publishing date	2024-04-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article ; Conference proceedings
ZDB-ID	2222993-0
ISSN	1861-9010 ; 1861-9002
ISSN (online)	1861-9010
ISSN	1861-9002
DOI	10.1055/s-0044-1785240
Database	Thieme publisher's database

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Zs.A 6479: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.A 6479/X: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)

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Article: Microglial Activation Is Associated With Vasoprotection in a Rat Model of Inflammatory Retinal Vasoregression.

Riemann, Sarah / Kolibabka, Matthias / Busch, Stephanie / Lin, Jihong / Hoffmann, Sigrid / Gretz, Norbert / Feng, Yuxi / Wohlfart, Paulus / Hammes, Hans-Peter

Frontiers in physiology

2021 Volume 12, Page(s) 660164

Abstract: Vascular dysfunction and vasoregression are hallmarks of a variety of inflammatory central nervous system disorders and inflammation-related retinal diseases like diabetic retinopathy. Activation of microglia and the humoral innate immune system are ... ...

Abstract	Vascular dysfunction and vasoregression are hallmarks of a variety of inflammatory central nervous system disorders and inflammation-related retinal diseases like diabetic retinopathy. Activation of microglia and the humoral innate immune system are contributing factors. Anti-inflammatory approaches have been proposed as therapies for neurovascular diseases, which include the modulation of microglial activation. The present study aimed at investigating the effects of microglial activation by clodronate-coated liposomes on vasoregression in a model of retinal degeneration. Clodronate treatment over 5 weeks led to an increase in activated CD74
Language	English
Publishing date	2021-04-26
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.660164
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Article ; Online: pdx1 Knockout Leads to a Diabetic Nephropathy- Like Phenotype in Zebrafish and Identifies Phosphatidylethanolamine as Metabolite Promoting Early Diabetic Kidney Damage.

Wiggenhauser, Lucas M / Metzger, Lena / Bennewitz, Katrin / Soleymani, Silas / Boger, Mike / Tabler, Christoph T / Hausser, Ingrid / Sticht, Carsten / Wohlfart, Paulus / Volk, Nadine / Heidenreich, Elena / Buettner, Michael / Hammes, Hans-Peter / Kroll, Jens

Diabetes

2022 Volume 71, Issue 5, Page(s) 1073–1080

Abstract: The pdx1-/- zebrafish mutant was recently established as a novel animal model of diabetic retinopathy. In this study, we investigate whether knockout of pdx1 also leads to diabetic kidney disease (DKD). pdx1-/- larvae exhibit several signs of early DKD, ... ...

Abstract	The pdx1-/- zebrafish mutant was recently established as a novel animal model of diabetic retinopathy. In this study, we investigate whether knockout of pdx1 also leads to diabetic kidney disease (DKD). pdx1-/- larvae exhibit several signs of early DKD, such as glomerular hypertrophy, impairments in the filtration barrier corresponding to microalbuminuria, and glomerular basement membrane (GBM) thickening. Adult pdx1-/- mutants show progressive GBM thickening in comparison with the larval state. Heterozygous pdx1 knockout also leads to glomerular hypertrophy as initial establishment of DKD similar to the pdx1-/- larvae. RNA sequencing of adult pdx1+/- kidneys uncovered regulations in multiple expected diabetic pathways related to podocyte disruption and hinting at early vascular dysregulation without obvious morphological alterations. Metabolome analysis and pharmacological intervention experiments revealed the contribution of phosphatidylethanolamine in the early establishment of kidney damage. In conclusion, this study identified the pdx1 mutant as a novel model for the study of DKD, showing signs of the early disease progression already in the larval stage and several selective features of later DKD in adult mutants.
MeSH term(s)	Animals ; Diabetes Mellitus/metabolism ; Diabetic Nephropathies/metabolism ; Female ; Glomerular Basement Membrane ; Humans ; Hypertrophy/metabolism ; Male ; Phenotype ; Phosphatidylethanolamines ; Podocytes/metabolism ; Zebrafish
Chemical Substances	Phosphatidylethanolamines ; phosphatidylethanolamine (39382-08-6)
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db21-0645
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Article ; Online: Comparison of metabolic and mitogenic response in vitro of the rapid-acting insulin lispro product SAR342434, and US- and EU-approved Humalog®.

Korn, Marcus / Wohlfart, Paulus / Gossas, Thomas / Kullman-Magnusson, Mari / Niederhaus, Birgit / Dedio, Juergen / Tennagels, Norbert

Regulatory toxicology and pharmacology : RTP

2019 Volume 109, Page(s) 104497

Abstract: SAR342434 is a biosimilar of insulin lispro (Humalog® U-100). Batches of SAR342434 were compared with Humalog® batches of either EU or US origin in a panel of in vitro biological assays that included insulin binding to insulin receptor (IR) isoforms A ( ... ...

Abstract	SAR342434 is a biosimilar of insulin lispro (Humalog® U-100). Batches of SAR342434 were compared with Humalog® batches of either EU or US origin in a panel of in vitro biological assays that included insulin binding to insulin receptor (IR) isoforms A (IR-A) and B (IR-B) and IR-A/IR-B autophosphorylation. A surface plasmon resonance biosensor-based assay was developed to characterize the kinetics of insulin binding to solubilized full-length IR-A or IR-B. Insulin-dependent metabolic activity assays included inhibition of lipolysis in in vitro differentiated human adipocytes, glucose uptake in L6-myocytes, and repression of glucose-6-phosphatase gene expression in human hepatocytes. Mitogenic activity assays included insulin binding to insulin-like growth factor-1 receptor (IGF1R), IGF1R autophosphorylation, and cell proliferation in MCF-7 cells. Weighted geometric means and their respective 95% confidence intervals (CI) were calculated for all 50% inhibitory or effective concentration values and kinetic binding constants for IR-A and IR-B. Statistical evaluation of the data demonstrated that the 90% CIs of the ratio of geometric means between SAR342434 and Humalog® EU or Humalog® US were within the predefined acceptance limits for each assay. Insulin lispro as SAR342434 solution demonstrated similarity to both US- and EU-approved Humalog® based on a side-by-side biological similarity assessment.
MeSH term(s)	Adipocytes ; Animals ; Antigens, CD/metabolism ; Biosimilar Pharmaceuticals/pharmacology ; CHO Cells ; Cell Line ; Cricetulus ; Drug Evaluation, Preclinical ; Humans ; Hypoglycemic Agents/pharmacology ; Insulin/metabolism ; Insulin Lispro/pharmacology ; Lipolysis/drug effects ; Mitosis/drug effects ; Receptor, Insulin/metabolism ; Recombinant Proteins/metabolism
Chemical Substances	Antigens, CD ; Biosimilar Pharmaceuticals ; Hypoglycemic Agents ; Insulin ; Insulin Lispro ; Recombinant Proteins ; SAR342434 ; INSR protein, human (EC 2.7.10.1) ; Receptor, Insulin (EC 2.7.10.1)
Language	English
Publishing date	2019-10-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	604672-1
ISSN	1096-0295 ; 0273-2300
ISSN (online)	1096-0295
ISSN	0273-2300
DOI	10.1016/j.yrtph.2019.104497
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Zs.A 1711: Show issues

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Article ; Online: The role of insulin resistance in experimental diabetic retinopathy-Genetic and molecular aspects.

Järgen, Patrick / Dietrich, Axel / Herling, Andreas W / Hammes, Hans-Peter / Wohlfart, Paulus

PloS one

2017 Volume 12, Issue 6, Page(s) e0178658

Abstract: Background: Diabetic retinopathy is characterized by defects in the retinal neurovascular unit. The underlying mechanisms of impairment-including reactive intermediates and growth-factor dependent signalling pathways and their possible interplay are ... ...

Abstract	Background: Diabetic retinopathy is characterized by defects in the retinal neurovascular unit. The underlying mechanisms of impairment-including reactive intermediates and growth-factor dependent signalling pathways and their possible interplay are incompletely understood. This study aims to assess the relative role of hyperglycemia and hyperinsulinemia alone or in combination on the gene expression patterning in the retina of animal models of diabetes. Material and methods: As insulinopenic, hyperglycemic model reflecting type 1 diabetes, male STZ-Wistar rats (60mg/kg BW; i.p. injection at life age week 7) were used. Male obese ZDF rats (fa/fa) were used as type-2 diabetes model characterized by persisting hyperglycemia and transient hyperinsulinemia. Male obese ZF rats (fa/fa) were used reflecting euglycemia and severe insulin resistance. All groups were kept till an age of 20 weeks on respective conditions together with appropriate age-matched controls. Unbiased gene expression analysis was performed per group using Affymetrix gene arrays. Bioinformatics analysis included analysis for clustering and differential gene expression, and pathway and upstream activator analysis. Gene expression differences were confirmed by microfluidic card PCR technology. Results: The most complex genetic regulation in the retina was observed in ZDF rats with a strong overlap to STZ-Wistar rats. Surprisingly, systemic insulin resistance alone in ZF rats without concomitant hyperglycemia did not induce any significant change in retinal gene expression pattern. Pathway analysis indicate an overlap between ZDF rats and STZ-treated rats in pathways like complement system activation, acute phase response signalling, and oncostatin-M signalling. Major array gene expression changes could be confirmed by subsequent PCR. An analysis of upstream transcriptional regulators revealed interferon-γ, interleukin-6 and oncostatin-M in STZ and ZDF rats. CONCLUSIONS: Systemic hyperinsulinaemia without hyperglycemia does not result in significant gene expression changes in retina. In contrast, persistent systemic hyperglycemia boosts much stronger expression changes with a limited number of known and new key regulators.
MeSH term(s)	Acute-Phase Proteins ; Animals ; Complement Activation ; Diabetes Mellitus, Experimental/genetics ; Diabetes Mellitus, Experimental/metabolism ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Diabetic Retinopathy/genetics ; Diabetic Retinopathy/metabolism ; Eye Proteins/biosynthesis ; Eye Proteins/genetics ; Gene Expression Profiling ; Gene Expression Regulation ; Hyperglycemia/complications ; Hyperglycemia/genetics ; Hyperglycemia/metabolism ; Hyperinsulinism/complications ; Hyperinsulinism/genetics ; Hyperinsulinism/metabolism ; Insulin Resistance ; Male ; Oncostatin M/biosynthesis ; Oncostatin M/genetics ; Rats, Mutant Strains ; Rats, Wistar ; Retina/metabolism ; Signal Transduction
Chemical Substances	Acute-Phase Proteins ; Eye Proteins ; Oncostatin M (106956-32-5)
Language	English
Publishing date	2017-06-02
Publishing country	United States
Document type	Comparative Study ; Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0178658
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